Human-specific lncRNA TMEM9B-AS1 is downregulated in skeletal muscle of individuals with type 2 diabetes and regulates ribosomal biogenesis
Sen, I.; Smith, J. A. B.; Caria, E.; Savikj, M.; Lian, K.; Ellefsen, S.; Zierath, J. R.; Krook, A.
Show abstract
Long non-coding RNAs (lncRNAs) are important regulators of skeletal muscle physiology, with altered expression noted in several human diseases including type 2 diabetes. Here we report TMEM9B-AS1, a previously uncharacterized lncRNA, is downregulated in skeletal muscle of men with type 2 diabetes. Silencing of TMEM9B-AS1 in primary human myotubes attenuated protein synthesis, concomitant with reduced phosphorylation of ribosomal protein S6, a downstream target of ERK and mTOR pathways. Moreover, we provide evidence that TMEM9B-AS1 plays a pivotal role in the regulation of ribosomal biogenesis by facilitating mRNA stabilization of the transcription factor MYC through a direct physical interaction with the RNA-binding protein IGF2BP1. Disrupted ribosomal biogenesis resulting from TMEM9B-AS1 silencing is linked reduced skeletal muscle mass in type 2 diabetes, elucidating molecular mechanisms contributing to skeletal muscle loss in metabolic disease.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Single-nucleus transcriptomics reveals functional compartmentalization in syncytial skeletal muscle cells 97%
- Single-nucleus RNA-seq identifies transcriptional heterogeneity in multinucleated skeletal myofibers 96%
- Mapping PTBP splicing in human brain identifies targets for therapeutic splice switching including SYNGAP1 96%
Similar papers in this journal
- Transcriptional regulation of adipocyte lipolysis by IRF2BP2 95%
- DKC1-mediated pseudouridylation of rRNA targets hnRNP A1 to sustain IRES-dependent translation and ATF4-driven metabolic adaptation 95%
- Folate depletion induces erythroid differentiation through perturbation of de novo purine synthesis 95%
Similar papers in this journal
- MME+ fibro-adipogenic progenitors are the dominant adipogenic population during fatty infiltration in human skeletal muscle 95%
- Mitochondrial dysfunction drives a neuronal exhaustion phenotype in methylmalonic aciduria 95%
- Dual roles of mTORC1-dependent activation of the ubiquitin-proteasome system in muscle proteostasis 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.